不同厚度脱细胞猪皮作为微粒皮移植覆盖物治疗大面积烧伤的临床观察

目的观察不同厚度脱细胞猪皮作为自体微粒皮移植覆盖物治疗大面积烧伤的效果。方法随机选择15例大面积深度烧伤患者,其中男性12例,女性3例,年龄35～57岁。烧伤后3-7d行大面积切痂,7例覆盖中厚型脱细胞猪皮,8例覆盖全厚型脱细胞猪皮,将自体微粒皮涂抹于创面,植皮区与供皮区面积比均约为10：1,常规加压包扎。观察猪皮排异变化、微粒皮成活情况及愈后皮肤弹性及外观。结果术后5d脱细胞猪皮与手术创面粘贴良好;中厚型脱细胞猪皮于术后10d、全厚型脱细胞猪皮于术后2周左右脱水干燥;中厚型脱细胞猪皮于术后3周、全厚型脱细胞猪皮于术后1个月左右逐渐分批脱落：脱落后全厚型脱细胞猪皮组创面愈合率达90．3％±2．7％,明显优于中厚型脱细胞猪皮组的68．2％±29％（P〈0.05）：创面愈合后全厚型脱细胞猪皮组瘢痕较轻,外观及弹性优于中厚型脱细胞猪皮组。结论脱细胞猪皮替代异体皮作为微粒皮移植覆盖物．全厚型脱细胞猪皮优于中厚型脱细胞猪皮。     

异种输血--猕猴受输猪红细胞的初步研究

本研究的目的是改造猪红细胞（pRBC）表面抗原，使之与灵长类动物相容，以探讨异种输血的可能性。结合使用α半乳糖苷酶（AGL）酶解和甲氧基聚乙二醇（mPEG）修饰改造猪红细胞表面异种抗原，并输注给猕猴，观察pRBC在猕猴体内活存时间及安全性；使用免疫抑制剂（蛇毒因子CVF和地塞米松）延长pRBC在猕猴体内的存活时间；建立失血性贫血猕猴模型，观察输注pRBC治疗失血性贫血猕猴的可能性。结果表明：AGL酶解能够去除猪红细胞表面主要异种抗原（α—Gal抗原），减弱其与猕猴血清的凝集反应，酶解技术与mPEG修饰技术结合可以使猪红细胞与猕猴血清更为相容。异种输血试验表明，双修饰的pRBC在猕猴体内存活时间为12小时，使用免疫抑制剂后，可延长至40小时；pRBC在猕猴体内8小时的存活率为38％，在输注pRBC的8小时内，失血猕猴的血红蛋白和红细胞压积可维持在失血前的正常水平。结论：改造后的pRBC可安全地输注给猕猴，改善失血猕猴的贫血症状．提示用猪红细胞进行异种输血是可能的。     

异种去细胞真皮基质在体内转归的初步研究

目的 初步研究异种（猪）去细胞真皮基质在体内的转归。方法 经曲通（Triton）X-100、胰蛋白酶处理得到异种（猪）去细胞真皮基质后，将其包埋于SD大鼠皮下，于术后1、2、4、6、8、12、16、20和30周观察异种（猪）去细胞真皮基质的大体形态及组织学变化。结果 制备的异种（猪）去细胞真皮基质去细胞成分，胶原纤维排列有序，基底膜结构完整。大体观察异种（猪）去细胞真皮基质原始形态随时间延长而逐渐模糊．组织学观察异种（猪）去细胞真皮基质1周以炎性细胞浸润为主，以后成纤维细胞、毛细血管逐渐增多，真皮胶原排列逐渐规则、致密。结论 异种（猪）去细胞真皮基质可在体内作为支架长期存在，并可诱导自身成纤维细胞及毛细血管有序长入。     

四种常用消毒剂对猪副粘病毒的灭活效果研究

目的观察4种化学消毒剂对猪副粘病毒的灭活效果,以便为畜牧业消毒提供参考。方法采用悬液定量杀菌试验与鸡胚感染检测方法对含碘、含氯、过氧乙酸和苯扎溴铵等4种消毒剂灭活猪副粘病毒的效果进行了实验室研究。结果以含有效碘30 mg/L的碘伏溶液,2000 mg/L过氧乙酸溶液,含有效氯25 mg/L的复方二氯异氰尿酸钠溶液以及含1000 mg/L苯扎溴铵消毒液对悬液内猪副粘病毒作用5 min以上,均可达到完全灭活。结论本试验4种常用化学消毒剂在较低浓度条件下,可以快速灭活猪副粘病毒,可用于对环境消毒和防止猪副粘病毒的传播。     

Novel Porcine Circoviruses in View of Lessons Learned from Porcine Circovirus Type 2-Epidemiology and Threat to Pigs and Other Species

Porcine circovirus type 2 (PCV2) plays a key role in PCV2-associated disease (PCVAD) etiology and has yielded significant losses in the pig husbandry in the last 20 years. However, the impact of two recently described species of porcine circoviruses, PCV3 and PCV4, on the pork industry remains unknown. The presence of PCV3 has been associated with several clinical presentations in pigs. Reproductive failure and multisystemic inflammation have been reported most consistently. The clinical symptoms, anatomopathological changes and interaction with other pathogens during PCV3 infection in pigs indicate that PCV3 might be pathogenic for these animals and can cause economic losses in the swine industry similar to PCV2, which makes PCV3 worth including in the differential list as a cause of clinical disorders in reproductive swine herds. Moreover, subsequent studies indicate interspecies transmission and worldwide spreading of PCV3. To date, research related to PCV3 and PCV4 vaccine design is at early stage, and numerous aspects regarding immune response and virus characteristics remain unknown.     

Gadolinium chloride-induced improvement of postischemic hepatic perfusion after warm ischemia is associated with reduced hepatic endothelin secretion

Selective Kupffer cell blockade by gadolinium chloride (GdCl₃) pretreatment of liver donors previously proved to be effective in reducing ischemia/reperfusion injury in rat liver transplants. Physiological mechanisms of this effect have not been specified so far. Vasoactive peptides are involved in liver blood flow regulation. We tested the hypothesis, that hepatic hemodynamic effects of GdCl₃ pretreatment are mediated by intrahepatic endothelin‐1 (ET) secretion in a standardized porcine model of warm liver ischemia and reperfusion. Standardized warm hepatic ischemia (45 min) was induced after laparotomy in intubation narcoses (ITN) by Pringle‐maneuver in pigs (n = 12). Animals were either pretreated with GdCl₃ (20 mg/kg i.v.) or sodium chloride 0.9% (control group) in a randomized manner 24 h before investigation. Relaparotomy was performed at day 7. Before, during ischemia and until 6 h after liver reperfusion, transhepatic blood flow (portal venous + hepatic artery flow) was defined by ultrasonic flow probes and hepatic parenchymous microcirculation evaluated by implanted thermodiffusion electrodes. ET plasma concentrations were analyzed (commercial RIA) at all time points in the hepatic veins after selective canulation. GdCl₃ pretreatment of animals markedly improved hepatic macro‐ and microperfusion before and particularly after warm ischemia. Mean ET plasma concentrations in the hepatic vein were significantly lower before, 6 h and 7 days after ischemia, compared with controls. Kupffer cell destruction by GdCl₃ pretreatment improves hepatic micro‐ and macroperfusion after warm ischemia, thus indicating reduced ischemia/reperfusion injury. Documented reduction of postischemic liver blood flow impairment after GdCl₃ pretreatment could be mediated by a decreased hepatic ET secretion, as hemodynamic effects were associated with significantly reduced ET plasma levels in hepatic veins.     

选择性脱细胞猪皮研制及早期临床应用

目的介绍选择性脱细胞猪皮覆盖大面积烧伤早期创面的研制方法及临床应用效果. 方法 2001年1月～2002年5月,对1例深Ⅱ度15%、Ⅲ度25%烧伤患者的右前臂和右小腿,行选择性脱细胞中厚猪皮早期覆盖.戊二醛交联后表皮面黏贴于容器,边缘包埋.在含0.25%胰酶的PBS液中37℃消化2小时,去污剂处理24小时后,漂洗备用.将处理后猪皮应用于1例切削痂自体微粒植皮创面覆盖约2%,大体和光镜观察其功能和外观恢复情况. 结果组织学观察见表皮层基本完整,真皮内无细胞.初步临床观察显示,选择性脱细胞猪皮的真皮可在创基成活,失活表皮可被宿主自体表皮替代. 结论选择性脱细胞猪皮有望替代现有材料用于大面积烧伤切削痂创面的早期覆盖.     

Platelet activation and hypercoagulability following treatment with porcine factor VIII (HYATE:C)

Activation of platelets and coagulation in vivo was studied in nine patients with hemophilia A and inhibitors to human Factor VIII, prior to and following treatment with porcine Factor VIII (PFVIII; HYATE:C). In addition, six hemophiliac patients were similarly studied after treatment with recombinant Factor VIII (rFVIII). Platelet activation was also examined in vitro using porcine von Willebrand factor (PvWF)-enriched and PvWF-depleted fractions obtained by fractionation of PFVIII. Coagulation was assessed by measuring the concentrations of plasma prothrombin fragment 1+2 concentrations (prothrombinase generation) and Factor Xa-ATIII. Patients treated with PFVIII had significantly increased numbers of circulating platelets expressing CD62 and CD63 (markers of platelet activation) and annexin V (marker of platelet procoagulant activity) compared to patients treated with rFVIII; the former patients also demonstrated an increase in plasma coagulability after therapy. In in vitro experiments it was observed that the platelet-activating and procoagulant capacity of PFVIII resided in the PvWF-enriched fraction, and the same was true for the plasma hypercoagulability following exposure of platelets to PFVIII. These results support the hypothesis that PFVIII-induced platelet activation provides a mechanism for enhancing hemostasis, separate from, and additional to, that due to increased circulating Factor VIII, and it is due to residual PvWF in the PFVIII preparation.